Transcatheter approaches to non-valvar structural heart disease

With advancement in transcatheter technology, numerous non-congenital structural heart lesions previously untreated, or treated with surgery are now amenable to transcatheter therapy. These therapies have centered on transcatheter valve replacement, however, other lesions are increasingly treated via the percutaneous approach. These procedures include patent foramen ovale closure, left atrial appendage occlusion, closure of post-infarct ventricular septal defects, occlusion of ruptured sinus of Valsalva aneurysm and treatment of paravalvar leaks. This review will outline indications for and approach to each of these procedures in the context of the current literature base with emphasis on pre- and intra-procedural imaging modalities.     

Transcatheter closure of unroofed coronary sinus using covered stents in an adult with drainage of the coronary sinus to the right ventricle after supra‐annular tricuspid valve replacement

We present a rare case of unroofed coronary sinus in a patient who underwent supra‐annular tricuspid valve replacement with consequent drainage of the coronary sinus to the right ventricle. It is unclear whether the coronary sinus was unroofed congenitally or iatrogenically. This rare setup resulted in significant cyanosis. The abnormal drainage was successfully closed via trans‐catheter delivery of covered stents with resolution of the cyanosis. © 2017 Wiley Periodicals, Inc.     

Transcatheter closure of congenital and acquired muscular ventricular septal defects using the Amplatzer device

Surgical closure of congenital or post-myocardial infarction (MI) muscular ventricular septal defect (MVSD) is associated with significant mortality and morbidity; therefore, both surgeons and cardiologists would welcome a safe non-surgical approach. The aim of this study is to report the combined experience of 2 cardiac centers in the transcatheter occlusion of both congenital and acquired MVSDs using the Amplatzer MVSD occluder device (AGA Medical Corporation, Golden Valley, Minnesota). Thirty-two patients underwent attempted transcatheter closure of an MVSD. Nineteen of these patients had congenital unoperated MVSD, twelve had post-MI MVSD and 1 patient had an acquired VSD post-surgical repair of hypertrophic cardiomyopathy. The median age of patients was 11.5 years (range, 0.1 86.0 years) and median weight was 34.5 kg (3.4 123.0 kg). All patients had significant shunt documented by echocardiography with a median Qp/Qs ratio of 1.7 (range, 1.0 5.3). The VSD location was mid-muscular in 14 patients, posterior in 10, apical in 5 and anterior in 3. The systolic pulmonary artery pressure ranged from 10 85 mmHg (median, 34.5 mmHg). The device was implanted successfully in 30 patients. The device size ranged from 6 26 mm (2 of these were ASD devices). There was immediate complete closure of the defect in 15 patients and 14 patients had residual shunt (foaming through the device). The median fluoroscopy time was 56.7 minutes (range, 11.7 146.0 minutes). Complications included: tamponade in 1 patient resulting in death; device malposition in 1 patient requiring surgical removal; severe hemolysis in 2 patients; and transient junctional rhythm in 1 patient. Among the 30 patients with successful implantation, three died in the hospital and 2 died later. On follow-up evaluation, there were no episodes of endocarditis, thromboembolism, hemolysis or wire disruption. We conclude that the Amplatzer MVSD occluder is a safe and effective device for closure of MVSDs up to 14 mm in diameter. Further clinical trials with this device are underway.     

Early ECG Abnormalities Associated with Transcatheter Closure of Atrial Septal Defects Using the Amplatzer® Septal Occluder

Conduction abnormalities and arrhythmias may occur in patients following secundum atrial septal defect (ASD) closure using the Amplatzer® septal occluder (ASO). Therefore, the aim of this study was to prospectively perform ambulatory ECG monitoring to assess the electrocardiographic effects of transcatheter closure (TCC) of ASD using the ASO device.From 5/97 to 3/99, 41 patients with secundum ASD, underwent TCC using the ASO device at a median age of 9.2[emsp4 ]y. (0.5–87[emsp4 ]y.) and median weight of 34[emsp4 ]kg (5.6–88[emsp4 ]kg.). Ambulatory Holter monitoring was performed pre- and immediately post TCC. Holter analysis included heart rate (HR), ECG intervals, supraventricular ectopy (SVE), ventricular ectopy (VE), and AV block.No change in baseline rhythm was noted in 37 patients (90%). Changes in AV conduction occurred in 3 patients (7%), including intermittent second degree AV block type II, and complete AV dissociation post closure. SVE was noted in 26 patients (63%) post closure, ranging from 5–2207 supraventricular premature beats (SVPB), including 9 patients (23%) with non-sustained supraventricular tachycardia (SVT), 3 of whom had short runs of SVT prior to closure. A significant increase in post-closure number of SVPB per hour (p=0.047) was noted. No significant difference was noted in PR interval, ventricular premature beats per hour, or QRS duration. Conclusions: Based on ambulatory ECG analysis, TCC of ASD with the ASO device is associated with an acute increase in SVE and a small risk of AV conduction abnormalities, including complete heart block. Long term follow-up studies will be necessary to determine late arrhythmia prevalence and relative frequency compared with standard surgical ASD repair.     

Use of intracardiac echocardiography to guide catheter closure of atrial communications

Intracardiac echocardiography (ICE) is slowly replacing transesophageal echocardiography as the preferred imaging tool to guide device closure of atrial septal defects and patent foramen ovale. This article is a brief review of the literature related to ICE, the technical aspects ICE imaging, techniques for obtaining the standard views, and the future directions of this methodology.     

Intermediate follow-up following intravascular stenting for treatment of coarctation of the aorta.

BACKGROUND: We report a multiinstitutional study on intermediate-term outcome of intravascular stenting for treatment of coarctation of the aorta using integrated arch imaging (IAI) techniques. METHODS AND RESULTS: Medical records of 578 patients from 17 institutions were reviewed. A total of 588 procedures were performed between May 1989 and Aug 2005. About 27% (160/588) procedures were followed up by further IAI of their aorta (MRI/CT/repeat cardiac catheterization) after initial stent procedures. Abnormal imaging studies included: the presence of dissection or aneurysm formation, stent fracture, or the presence of reobstruction within the stent (instent restenosis or significant intimal build-up within the stent). Forty-one abnormal imaging studies were reported in the intermediate follow-up at median 12 months (0.5-92 months). Smaller postintervention of the aorta (CoA) diameter and an increased persistent systolic pressure gradient were associated with encountering abnormal follow-up imaging studies. Aortic wall abnormalities included dissections (n = 5) and aneurysm (n = 13). The risk of encountering aortic wall abnormalities increased with larger percent increase in CoA diameter poststent implant, increasing balloon/coarc ratio, and performing prestent angioplasty. Stent restenosis was observed in 5/6 parts encountering stent fracture and neointimal buildup (n = 16). Small CoA diameter poststent implant and increased poststent residual pressure gradient increased the likelihood of encountering instent restenosis at intermediate follow-up. CONCLUSIONS: Abnormalities were observed at intermediate follow-up following IS placement for treatment of native and recurrent coarctation of the aorta. Not exceeding a balloon:coarctation ratio of 3.5 and avoidance of prestent angioplasty decreased the likelihood of encountering an abnormal follow-up imaging study in patients undergoing intravascular stent placement for the treatment of coarctation of the aorta. We recommend IAI for all patients undergoing IS placement for treatment of CoA.